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Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10 weeks of endurance training

PURPOSE: The endurance training (ET)-induced increases in peak oxygen uptake ([Formula: see text] O(2peak)) and cardiac output ([Formula: see text] (peak)) during upright cycling are reversed to pre-ET levels after removing the training-induced increase in blood volume (BV). We hypothesised that ET-...

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Detalles Bibliográficos
Autores principales: Skattebo, Øyvind, Bjerring, Anders Wold, Auensen, Marius, Sarvari, Sebastian Imre, Cumming, Kristoffer Toldnes, Capelli, Carlo, Hallén, Jostein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7181565/
https://www.ncbi.nlm.nih.gov/pubmed/32172291
http://dx.doi.org/10.1007/s00421-020-04336-2
Descripción
Sumario:PURPOSE: The endurance training (ET)-induced increases in peak oxygen uptake ([Formula: see text] O(2peak)) and cardiac output ([Formula: see text] (peak)) during upright cycling are reversed to pre-ET levels after removing the training-induced increase in blood volume (BV). We hypothesised that ET-induced improvements in [Formula: see text] O(2peak) and [Formula: see text] (peak) are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O(2) difference (a-[Formula: see text] O(2)diff; [Formula: see text] O(2)/[Formula: see text] ), cardiac dimensions and muscle morphology were studied to assess their role for the [Formula: see text] O(2peak) improvement. METHODS: Twelve untrained subjects ([Formula: see text] O(2peak): 44 ± 6 ml kg(−1) min(−1)) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hb(mass)) and BV were assessed pre- and post-ET. [Formula: see text] O(2peak) and [Formula: see text] (peak) during upright and supine cycling were measured pre-ET, post-ET and immediately after Hb(mass) was reversed to the individual pre-ET level by phlebotomy. RESULTS: ET increased the Hb(mass) (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and [Formula: see text] O(2peak) during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in [Formula: see text] O(2peak) compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was [Formula: see text] (peak) (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased [Formula: see text] (peak) and a-[Formula: see text] O(2)diff accounted for 70% and 30% of the [Formula: see text] O(2peak) improvements, respectively. Markers of mitochondrial density (CS and COX-IV; P ≤ 0.007) and left ventricular mass (P = 0.027) increased. CONCLUSION: The ET-induced increase in [Formula: see text] O(2peak) was preserved despite removing the increases in Hb(mass) and BV by phlebotomy, independent of posture. [Formula: see text] O(2peak) increased primarily through elevated [Formula: see text] (peak) but also through a widened a-[Formula: see text] O(2)diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.